Competes with ethylene glycol for metabolism via alcohol dehydrogenase (ADH) enzyme. Diethylene glycol was once used as a vehicle for the drug sulphanilamide and when used for this it caused some 76 deaths. Thus, ethylene glycol is metabolized by several oxidation steps eventually to yield oxalic acid (figure 7.56). DEG is used as a component of multiple different products including antifreeze preparations, cosmetics, lubricants, brake fluids, wallpaper strippers, heating/cooling fuel and as a plasticizer. The rationale for the use of bicarbonate is the massive generation of acid by the metabolism of ethylene glycol. We found that strain JM37 grew rapidly with ethylene glycol as a … There are three recogniseable stages to ethylene glycol toxicity. Previous chapter: Urate and hippurate anions: their origins and clearance, Next chapter: Diabetic, alcoholic and starvation ketoacidosis. This deliciously syrupy tongue-pleasing alcohol is a favourite among the critically ill population. Several deaths are recorded annually in the U.S. alone. In this study, we investigated the metabolism of ethylene glycol in the Pseudomonas putida strains KT2440 and JM37 by employing growth and bioconversion experiments, directed mutagenesis, and proteome analysis. The clinical biochemical features reflect the biochemical and physiological effects. Fomepizole has an 8,000 fold greater binding affinity to ADH and thus prevents the metabolism of ethylene glycol to toxic acid metabolites. 1986 Nov;7(4):547-65. The elevated NADH to NAD ration causes the conversion of pyruvate pyruvate to lactate. b intravenous sodium bicarbonate; this corrects the acidosis—animal studies have shown that this increases the LD50 by around four times c calcium gluconate; this corrects the hypocalcaemia d dialysis to remove ethylene glycol. Of the various ways one can become acquainted with ethylene glycol, this is probably the most common. Ethylene glycol, the parent compound, is inebriating but generally considered nontoxic. Otherwise, much of it is metabolized into hideous daughter-compounds, which are also ex… However, like all other glycols it is is rapidly absorbed, even through the gastric mucosa. (See supplemental page for metabolic pathway figures for ethylene glycol and methanol). 1986 Apr;33(2):311-23. It is not well absorbed through the skin; nor does it evaporate particularly well. These toxic substances also affect the cardiopulmonary system and can cause renal failure. If ingestion was recent (1-2 hours), vomiting is induced and activated charcoal is given to reduce further absorption of the ethylene glycol. Glycolic acid (GA) and ethylene glycol (EG) are versatile two-carbon organic chemicals used in multiple daily applications. Ingestion of sufficient amounts is fatal if untreated. The lungs show oedema, and occasionally calcium oxalate crystals and degenerative myocardial changes may also occur. OVERVIEW >1 mL/kg or a mouthful in a child is potentially lethal ethylene glycol itself is relatively non-toxic -> metabolites extremely toxic (glycolate) rate limiting step = alcohol dehydrogenase activity accumulation of glycolate -> direct cellular toxicity CLINICAL FEATURES drunk: automotive antifreeze, solvent, polish, paints, cosmetics, brake fluid, car wash fluid. Thus, after standard procedures such as gastric lavage to reduce absorption and supportive therapy for shock and respiratory distress, patients are treated with the following: a ethanol; this competes with ethylene glycol for alcohol dehydrogenase, but as it is a better substrate the first step in ethylene glycol metabolism is blocked—animal studies have shown that this doubles the LD50. In 1977, Clay and Murphy poisoned some monkeys and revealed that the serum bicarbonate levels decreased in proportion to rising glycolic acid levels. In the parlance of the street cop, this equates to a blood alcohol level of 0.1%, twice the legal driving limit in Australia. Fig: Metabolism of Ethylene Glycol . The extra osmoles represent some mixture of ethylene glycol and glycolic acid, eagerly water-soluble, and thus rapidly dialysed. Well. In clinical practice, poisoning with ethylene glycol, methanol, and isopropyl alcohol is common. Ethylene glycol metabolism generates glycolate, which can be mistaken for lactate by portable lab assays utilizing lactate oxidase. The next stage is that of cardiac toxicity. Thus, there is reduced plasma bicarbonate, low plasma calcium and raised potassium. The chief diagnostic feature of ethylene glycol toxicity (apart from doing an actual ethylene glycol level) is calcium oxalate crystals in the urine. Such a thing indeed exists, but is not well studied. ternative metabolism of toxic alcohols to non-toxic metabolites. In contrast, the conversion of glycolic acid to glyoxylic acid is slower and is the rate-limiting step in the metabolism of ethylene glycol. Ethylene glycol and its toxic acid metabolytes, "On the metabolic acidosis of ethylene glycol intoxication.". As it has a sweet. There is thus an increase in the level of lactate and lactic acidosis may result. Anything over 1.0-1.5mg/kg is considered lethally toxic. The mechanism of toxicity of ethylene glycol involves metabolism, but unlike previous examples this does not involve metabolic activation to a reactive metabolite. Aldehyde dehydrogenase causes glyceraldhyde to become glycolic acid. First you may feel slightly drunk for about 4 hours. Methanol is slowly metabolised to formaldehyde which is rapidly metabolised to formate, the metabolite mainly resp … The authors (who did not identify themselves) suggested a loading dose of 0.6g per kg body weight, or roughly 40g for a 70kg male, to get to 100mg/dL. However, there is one case series of three poor fools who have admitted to injecting alcohol (ranging from vodka to beer, dosage unknown) and whose veins did not suffer excessively as a consequence, in spite of what i can only assume was suboptimal injecting technique. The highest survived dose reported is 2 litres. Potentially, it may interact with things like disulfiram and metronidazole, which block acetaldehyde dehydrogenase. The initial intoxication is thought to occur much in the same way as ethanol intoxication, by acting on the GABA receptors. The most important initial treatment for ethylene glycol poisoning is stabilizing the person. Clay, Keith L., and R. C. Murphy. 1. In contrast to ethylene glycol, propylene glycol rarely causes toxic effects. An additional benefit is the effect of "ion trapping" formic acid. A Norfolk couple report that it tasted "horrible", though the husband finished his glass as a demonstration of his manliness. Mono Ethylene Glycol, commonly referred to as Ethylene Glycol Antifreeze but also referred to as Ethane-1,2-diol, MEG, EG and Industrial Glycol. Suppression of metabolism – fomepizole and IV ethanol are temporizing measures; Removal of toxin – haemodialysis; Alkalinisation in order to counteract metabolic acidosis (Na bicarbonate) Folic acid and folinic acid may be useful adjuncts (but does not directly improve patient’s clinical state) Ethylene glycol. Compared to ethylene glycol, ethanol had something like 100 times more affinity for alcohol dehydrogenase. Thus the treatment of poisoning with ethylene glycol is a logical result of understanding the biochemistry of the toxicity. The minimum lethal dose of ethylene glycol is about 100 ml and after ingestion death may occur within 24 h from damage to the CNS or more slowly (8-12 days) from renal failure. More bicarbonate must be added in order to buffer the excessive number of hydrogen ions present in the patient, so that H2O and CO2 may be generated. This treatment is only effective in do… The osmolar gap may be raised (to > 10) early in the course but this is variable. Glycolic acid is the smallest of the alpha-hydroxy acids, and is used in all sorts of skin-related industries (be it tanning, as a leather-dye, or as a part of dermatological skin peeling). Thus, this acidosis is "bicarbonate-resistant". The treatment of poisoning with ethylene glycol reflects the mechanism and biochemical effects. Otherwise, much of it is metabolized into hideous daughter-compounds, which are also excreted by the unhappy kidneys (which find themselves mangled by the process). Partially because lactic acidosis – –The first two steps in ethylene glycol metabolism cause the reduction of NAD to NADH. Traditionally, gastric lavage or nasogastric aspiration of gastric contents are the most common methods employed in ethylene glycol poisoning. "Ethylene glycol poisoning." However, like all other glycols it is is rapidly absorbed, even through the gastric mucosa. It and its toxic byproducts first affect the central nervous system, then the heart, and finally the kidneys. T he detection of calcium oxalate crystals in the urine is often stated to be a useful guide but this is wrong. 1) 4-methylpyrazole (4-MP)[Antizole or fomepazole]: This medication inactivates alcohol dehydrogenase. If untreated, ingestion of only 30 to 60 mls may be sufficient to cause permanent organ damage or death. Ethylene glycol is a precursor for many polymers, eg. Upon ingestion, ethylene glycol is oxidized to glycolic acid, which is, in turn, oxidized to oxalic acid, which is toxic. The parent compound is osmotically active, and is responsible for the increased osmolality observed in the early course of exposure prior to metabolism. A lot of this information comes from “Goodman & Gilman's The Pharmacological Basis of Therapeutics” 11th ed by Brunton et al,and   “Basic & Clinical Pharmacology” 11th ed. In patients exposed to ethylene glycol, 100mg thiamine and 100mg pyridoxine can be administered IV daily Apparently, it gives one a buzz similar to that of alcohol intoxication. The mechanism of metabolic acidosis is more interesting. 20. Only at the third admission, 2 years after the first, was the possibility of an underlying metabolic disorder considered. Then, you might feel slightly ill. As the glycolic acid begins to appear in the bloodstream, metabolic acidosis ensues and hyperventilation follows. The acetogenic bacterium Acetobacterium woodii is able to grow by the oxidation of diols, such as 1,2-propanediol, 2,3-butanediol, or ethylene glycol. polyethylene glycol. Once past this window of time, absorption has already occurred. Ipecac-induced Anything over 0.1ml/kg will require treatment. Clin Nephrol. This is mainly because A. Absorption of propylene glycol from the gastrointestinal tract is slow. C. Ethylene glycol is … Central nervous system depression is the most pronounced feature at this stage; the coma may be garnished with seziures. META Study Group". Common ethyl alcohol (ethanol) binds much more easily to ADH than ethylene glycol or methanol does. INTRAVENOUS INJECTION OF ALCOHOL BY DRUG INJECTORS: REPORT OF THREE CASES; "Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. Ethylene glycol's metabolites are responsible for the anion gap metabolic acidosis. "Methanol and ethylene glycol poisoning: a case study and review of current literature. The major danger is due to its sweet taste, which can attract children and animals. The first step is catalysed by the enzyme alcohol dehydrogenase and herein lies the key to treatment of poisoning. As ethylene glycol is rapidly absorbed, gastric decontamination is unlikely to be of benefit unless it is performed within 60 minutes of ingestion. It does what ethanol would do, except it does so with great expense, and without ethanol intoxication. Ameera S. Mahdi and Andrew J. McBride INTRAVENOUS INJECTION OF ALCOHOL BY DRUG INJECTORS: REPORT OF THREE CASES; Alcohol and Alcoholism (1999)  34(6): 918-919. It boils at 197 degrees C, in case you ever want to boil some. Lactate gap refers to the difference in lactate measurement via different methods: Elevated lactate on portable blood gas machine utilizing lactate oxidase. The mechanism of toxicity of ethylene glycol involves metabolism, but unlike previous examples this does not involve metabolic activation to a reactive metabolite. This effect rarely produces serious morbidity or death by itself.Acute renal failure as well as a severe anion-gap metabolic acidosis results from the metabolism of ethylene glycol into at least 4 distinct metabolites. There seem to be three recognizable clinical stages: a Within 30 min and lasting for perhaps 12 h, there is intoxication, nausea, vomiting, coma, convulsions, nystagmus, papilloedema, depressed reflexes, myoclonic jerks and tetanic contractions. It is not well absorbed through the skin; nor does it evaporate particularly well. Recurrent severe anion gap metabolic acidosis secondary to episodic ethylene glycol intoxication. The imbalance in the level of this in the body is adjusted by oxidation to NAD coupled to the production of lactate. "On the metabolic acidosis of ethylene glycol intoxication." The main indication for this (apart from the inevitable renal failure of a late presentation) is a high osmolar gap. DePass LR, Garman RH, Woodside MD, Giddens WE, Maronpot RR, Weil CS. The conversion to glycolic acid is somewhat rapid. How drunk do you have to be to prevent ethylene glycol metabolism? In this study, we investigated the metabolism of ethylene glycol in the Pseudomonas putida strains KT2440 and JM37 by employing growth and bioconversion experiments, directed mutagenesis, and proteome analysis. The treatment options here are discussed in brief. I cannot find the original paper, but a letter in response to it suggests one should sustain a blood ethanol concentration of 20 to 30 mmol/L (100 to 150 mg/dL). Thus, ethylene glycol is metabolized by several oxidation steps eventually to yield oxalic acid (figure 7.56). Hypocalcemia may occur as oxalate chelates the serum calcium. Diethylene glycol (DEG) is a clear, colorless, odorless liquid with a sweet taste, and is an excellent solvent for water-insoluble chemicals and drugs. Ethylene glycol (EG) poisoning is common in dogs and cats 1 – 4 and often results in death if it is not diagnosed and treated promptly. Toxicology and applied pharmacology 39.1 (1977): 39-49. 5 The mortality rate in dogs is reported to range from 59% to 70% 1, 5 and is thought to be even higher in cats. Henderson, William R., and Jeffrey Brubacher. There are two proposed mechanisms of propylene glycol metabolism: The first is as follows: Ethylene glycol is transformed in the liver by alcohol dehydrogenase to glyceraldehyde. "Methanol and ethylene glycol poisoning: a case study and review of current literature." Pollution from ethylene glycol, and plastics containing this monomer, represent a significant environmental problem. Parry, Michael F., and Ronald Wallach. Typically, people drink this stuff. b Between 12 and 24 h there is tachypnoea, tachycardia, hypertension, pulmonary oedema and congestive cardiac failure. These alcohol-related intoxications can present with high anion gap metabolic acidosis and increased osmolality. This increases its clearance, and keeps it out of the fatty central nervous system, where its effects are the most destructive (specifically, the effects on the tender juicy retina). DEG has also been inappropriately substituted in pharmaceutical preparations for nontoxic constituents, resulting in more than a dozen epidemics of human poisoning, with resultant … At this stage, there is no acidosis, but the anion gap is widened (unmetabolised ethylene glycol floods the bloodstream). Ethylene glycol is moderately toxic, with an oral LDLo = 786 mg/kg for humans. Methanol and ethylene glycol metabolism can be understood by first studying the metabolism of ethanol, which occurs in two steps: Ethanol is oxidized to acetaldehyde with production of NADH by alcohol dehydrogenase, an enzyme located, for the most part, in the cytosol of hepatocytes (see Chapter 24 ). Thge major interactions of ethylene glycol are with ethanol and fomepizole, which is put to good use in management of the toxicity. The American Journal of Medicine 57.1 (1974): 143-150. Roadmap To Genius Improve Intelligence & IQ, Candida Crusher Permanent Yeast Infection Solution, Glutathione conjugation - Metabolic Activation, Aromatic Hydroxylation - Metabolic Activation, Glucuronide formation - Metabolic Activation, Aliphatic Hydroxylation - Metabolic Activation, How to Cope with Acute Renal Failure Naturally. To summarize, you give massive amounts of bicarbonate, and then you either start an ethanol infusion, regular doses of fomepizole, or haemodialysis. The alcohols: ethanol, methanol, isopropanol, ethylene glycol. All animals are susceptible to ethylene glycol (EG) toxicity, but it is most common in dogs and cats. B. Propylene glycol is metabolized to more toxic compounds. These 95% commercial antifreeze preparations are diluted ~50% with water when used in vehicle cooling systems. Effective Treatments for Peripheral Neuropathy, Carpal Tunnel Syndrome Holistic Treatments Ebook, 7 Useful Tips for Improving Your Mental Focus, How to Lose Weight From Your Stomach Fast, An alternative approach to perioral rhytides, Mental Impotence Holistic Treatments Ebook, This substance is a liquid used in antifreeze, paints, polishes and cosmetics. There is a lot of good, thorough literature on the management of ethylene glycol toxicity. The contribution of all the other metabolites was negligible. It is first converted by alcohol dehydrogenase to glycoaldehyde, which is then metabolised to glycolic acid by aldehyde dehydrogenase. Chronic toxicity and oncogenicity studies of ethylene glycol in rats and mice. Clinical toxicology 36 (7): 659–66. There is degeneration of proximal tubular epithelium with calcium oxalate crystals and fat droplets detectable in tubular epithelial cells. The investigation of its microbial metabolism therefore provides insights into the environmental fate of this pollutant and also enables its utilization … The rate-limiting step of ethylene glycol metabolism is the ADH-catalyzed step. Alternatively, you may consider injecting it. GA and EG are currently produced by chemical synthesis, but their biotechnological production from renewable resources has received a substantial interest. Fundam Appl Toxicol. There is a complex metabolic pathway with multiple products, of which oxalic acid is the most dreaded. The degeneration of distal tubules may also be seen. The goal of specific treatment is to prevent the metabolism of ethylene glycol into the toxic metabolites. Elimination: Ethylene glycol has an elimination half-life of about 3 hours. 2003 Sep;60(3):205-10. 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